钛表面烤瓷的预氧化处理工艺研究

目的：考察预氧化处理工艺是否适合钛－瓷修复。方法：采用剪切实验法测试在未预氧化处理（Ｒ１），３００℃（Ｒ２）、５００℃（Ｒ３）及７００℃（Ｒ４）预氧化处理时钛－氧化处理时钛－瓷结合强度，并用金、相显微镜及电子探针分析各组的钛－瓷界面状况。结果：Ｒ１、Ｒ２、Ｒ３及Ｒ４各组剪切强度值分别为５０．２５±６．５２ＭＰａ、４４．６７±７．０８ＭＰａ、２７．６９±５．２７ＭＰａ和２２．５１±４．９０Ｍｐａ。界面分析表明，各组钛与瓷界面结合紧密、无裂隙，并存在元素扩散带，不同的是各组元素扩散带宽度不一，其规律是Ｒ１＜Ｒ２＜Ｒ３＜Ｒ４。结论：预氧化处理工艺不适合钛－瓷修复。     

微晶蜡非催化氧化反应的神经网络模型

对微晶蜡进行了非催化空气氧化，并利用人工神经网络将氧化微晶蜡的酸值、酯值及微晶蜡的氧化条件（反应温度、空气流量和反应时间）进行关联，建立了微晶蜡非催化氧化的酸值、酯值的神经网络模型，并用该模型预测了反应条件对微晶蜡氧化反应过程的影响。结果表明，该模型不但具有较高的计算精度，而且具有满意的预测能力。     

The Effect of Intensive Insulin Therapy on the Insulin-regulatable Glucose Transporter (GLUT4) Expression in Skeletal Muscle in Type 1 Diabetes

Studies in normal man and rodents have demonstrated that the expression of the dominant glucose transporter in skeletal muscle, GLUT4, is regulated by insulin at supraphysiological circulating levels. The present study was designed to determine whether intensified insulin replacement therapy for 24 h given to patients with Type 1 diabetes in poor metabolic control was associated with an adaptive regulation of GLUT4 mRNA and protein levels in vastus lateralis muscle. Nine Type 1 diabetic patients with a mean HbA_1c of 10.3% were included in the protocol. After intensified treatment with soluble insulin for 24 h the fasting plasma glucose concentration decreased from 20.8 ± 2.3 (SD) to 8.7 ± 2.3 mmol 1^?1 whereas the fasting serum insulin level increased from 0.06 ± 0.02 to 0.17 ± 0.09 nmol 1^?1 However, despite a 2.8-fold increase in serum insulin levels and more than a halving of the plasma glucose concentration for at least 15 h no significant alterations occurred in the amount of GLUT4 protein (0.138 ± 0.056, poor control vs 0.113 ± 0.026 arb. units, improved control, p = 0.16) or GLUT4 mRNA (96432 ± 44985, poor control vs 81395 ± 25461 arb. units, improved control, p = 0.54). These results suggest, that in spite of evidence that high insulin levels affect GLUT4 expression in muscle, changes in serum insulin within the physiological range do not play a major role in the short-term regulation of GLUT4 expression in Type 1 diabetic patients.     

The effect of harmaline on intestinal sodium transport and on sodium-dependentd-glucose transport in brush-border membrane vesicles from rabbit jejunum

Harmaline inhibition of sodium uptake and of sodium-dependentd-glucose transport was investigated using brush-border membrane vesicles from frozen rabbit jejunum. Under sodium-gradient conditions, initiald-glucose uptake (20 s) was inhibited by harmaline at concentrations above 0.5 mM, but at lower harmaline concentrationsd-glucose uptake was stimulated by 10–15%. When a similar potassium gradient was used, harmaline had no effect. At concentrations upt to 2 mM, harmaline did not alter the equilibrium uptake ofd-glucose ord-mannitol. After pre-equlibration with sodium (25 mM),d-glucose uptake was inhibited at harmaline concentrations ranging from 0.1 to 2 mM. Sodium (10 mM) uptake was also inhibited by harmaline. Increasing the sodium concentration reduced the inhibitory effect of harmaline on tracer sodium uptake as well as on sodium-dependentd-glucose uptake. Similar to phlorizin, harmaline (1 mM) was able to prevent glucose-induced sodium influx across the brush-border membrane.Sodium uptake into brush-border membrane vesicles seems to be inhibited at lower harmaline concentrations than sodium-dependentd-glucose uptake. At high (2 mM) inhibitor concentrations, however, sodium-dependent glucose uptake is more strongly inhibited than sodium uptake. These results suggest that harmaline inhibits both sodium and sodium-dependent transport across intestinal brush-border membranes by interacting with specific sodium-binding sites.     

Glucosamine-resistant mutations in yeast affecting the glucose repression sensitivity of electron transport enzymes

Summary We have isolated two mutant strains, GSA^r-4 and GSA^r-5, which are able to grow on lactate in the presence of D-glucosamine. The glucosamine-resistant phenotype results from the cooperative effects of mutations in three loci, GAR1, GAR2 and GAR3. Both glucosamine resistant mutant strains were doubly mutant at gar1 gar2 (GSA^r-4) or gar1 gar3 (GSA^r-5). The mutants were also shown to exhibit glucose repression insensitive synthesis of NADH-cytochrome c reductase and cytochrome c oxidase. Glucose-repressible synthesis of the following enzymes was seen: succinic dehydrogenase, succinic: cytochrome c reductase, maltase (PNPGase), galactokinase, -galactokinase. The glucose-repression insensitivity segregates in association with the glucosamine resistance.     

Influence of glucose ingestion by humans during recovery from exercise on substrate utilisation during subsequent exercise in a warm environment

Carbohydrate (CHO) ingestion during short-term recovery from prolonged running has been shown to increase the capacity for subsequent exercise in a warm environment. The aim of this study was to examine the effects of the amount of glucose given during recovery on substrate storage and utilisation during recovery and subsequent exercise in a warm environment. A group of 11 healthy male volunteers took part in two experiments in a controlled warm environment (35°C, 40% relative humidity), 1 week apart. On each occasion the subjects completed two treadmill runs (T1 and T2) at a speed equivalent to 60% of maximal oxygen uptake, for 90 min, until they were fatigued, or until aural temperature (T _aur) reached 39°C. The two runs were separated by a 4 h recovery period (REC), during which subjects consumed 55 g of naturally enriched [U-¹³C]-glucose in the form of a 7.5% carbohydrate-electrolyte solution (CES, mass of solution 667 g) immediately after T1. The subjects then consumed either: the same quantity of CES, or an equivalent volume of an electrolyte placebo, at 60, 120 and 180 min during REC, providing a total of 220 g (C220) or 55 g (C55) of [U-¹³C]-glucose, respectively. Expired gases were collected at 15 min intervals during exercise and 60 min intervals during REC, for determination of total CHO and fat oxidation by indirect respiratory calorimetry, and orally ingested [U-¹³C]-glucose oxidation, estimated from the ¹³C:¹²C ratio of expired CO₂. Substrate metabolism did not differ between conditions during T1. Despite the fact that total CHO (P<0.05) and ingested glucose oxidation (P<0.01) were greater during REC of the C220 condition, glycogen synthesis was estimated to be approximately fivefold greater (P<0.01) than in the C55 condition. During T2 the rate of total CHO oxidation was higher (P<0.01) and total fat oxidation lower (P<0.01) at all times during the C220 compared to the C55 condition. The greater CHO oxidation during C220 appeared to be met from ingested sources, as the rate of [U-¹³C]-glucose oxidation was greater (P<0.01) at all times during T2, compared to C55. Whilst more of the ingested substrate remained unoxidised on completion of T2 during C220, exercise duration was similar in the two experimental conditions, and was limited by thermoregulatory incapacity (T _aur>39°C) rather than substrate availability per se. Electronic Publication     

Glucose preferences in wild and domestic guinea pigs

Male wild (Cavia aperea) and domestic (C. porcellus) guinea pigs were tested in two-bottle choice tests for preferences between glucose solutions of different concentrations and de-ionized water. Wild males showed significant preferences for concentrations between 0.025 and 0.4 M glucose while domestic males preferred only the 0.2 M glucose solution to de-ionized water. C. aperea males also consumed significantly greater volumes of liquid per kg body $\text{wt.}{}^{\mathrm{<mtext>3</mtext><mtext>4</mtext>}}$ during the glucose tests than did the C. porcellus males. These comparative results contrast sharply with those obtained by other authors with wild and domestic Norway rats.     

p-Amino salicylic acid — oxidized cellulose system: a model for long term drug delivery

The immobilization of p-amino salicylic acid (PASA) on periodic oxidized cellulose (O.C) as a biocompatible carrier was investigated. The immobilization of the PASA is based on Schiff's base formation between the amino group of PASA and the aldehyde group of O.C. The in vivo and in vitro release of p-amino salicylic acid was studied. Such a system may be useful for the sustained delivery of the drugs in the body, since O.C. itself is a biosoluble carrier.     

Hypothalamic sensitivity to 2-deoxy-D-glucose and glucose: effects on feeding behavior

The effect on food intake of intrahypothalamic deposition of glucose or the glucose metabolic inhibitor 2-deoxy-D-glucose was studied to determine the function of the often hypothesized hypothalamic glucoreceptors in feeding behavior. Our results suggest that the lateral hypothalamic region, as well as the medial hypothalamus, contain glucoreceptive cells that form part of a feeding system.     

Rapid activation of glycogen synthase and protein phosphatase in human skeletal muscle after isometric contraction requires an intact circulation

The effects of isometric contraction (66% of maximal force) and recovery on glycogen synthase fractional activity (GSF) in human skeletal muscle have been studied. Biopsies were taken from the quadriceps femoris muscle at rest, at fatigue and 5 min postexercise on two occasions: after one of the contractions, the circulation to the thigh was occluded during the 5 min recovery (OCC), and after the other contraction, the circulation was intact (control, CON). During CON, GSF decreased from (mean ± SE) 0.34±0.05 at rest to 0.24±0.02 at fatigue and then increased to 0.74±0.04 at 5 min postexercise; corresponding values for OCC were 0.37±0.04, 0.25±0.04 and 0.48±0.05 (P<0.001 vs. CON for 5 min postexercise only). Compared with the value at fatigue, protein phosphatase activity (PP) increased by 79±16% during CON recovery (P<0.01), whereas no change was observed during OCC recovery. Uridine diphosphate glucose increased by approximately 2.5-fold at fatigue, remained elevated during OCC recovery, but reverted to the preexercise level during CON recovery (P<0.001 vs. OCC recovery). Glucose 6-P increased approximately 5-fold at fatigue and was higher at 5 min postexercise in OCC vs. CON recovery (8.6±1.5 vs. 4.1±0.9 mmol/kg dry wt; P<0.01). It is concluded that the rapid increase in GSF after intense exercise with an intact circulation may be at least partly attributed to an increase in the specific activity of PP. The increase in GSF during recovery in OCC may be at least partly attributed to the high glucose 6-P content in vivo, which enhances the substrate suitability of GS for PP. Thus, separate mechanisms exist for the activation of PP and GS during recovery from intense short term exercise.